Scabies is a contagious ectoparasitic dermatosis caused by Sarcoptes scabiei var. hominis. It is characterized by intense pruritus, often worse at night, and a variable eruption of papules, vesicles, burrows, nodules, and secondary excoriations. The disease disproportionately affects children and adolescents living in socially disadvantaged or overcrowded settings, where prolonged skin-to-skin contact and delayed recognition promote transmission. Congregate living environments, including residential schools and boarding facilities, therefore represent important settings for transmission, reinfestation, and outbreak propagation. Recent clinical reviews emphasize that careful history-taking regarding close contacts and living conditions remains central to scabies assessment, alongside a complete dermatological examination ^1–3.

Despite the common involvement of interdigital areas, flexural wrists, axillae, waistlines, buttocks, perineum, and genitals in classical scabies, the morphology and distribution can vary due to chronic rubbing, past treatments, eczematization, and infections. Such changes can make identification of scabetic lesions more difficult and pose challenges in diagnosis at the bedside level, especially when the active lesions consist predominantly of scratched papules, erosions, crusts, and post-inflammatory hyperpigmentation. Identification through microscopy of mites, eggs, and scybala, and dermoscopy where possible, can aid in diagnosis; but it may still be required in cases where such means are not available. Current guidelines still recommend treatment of the suspect cases and joint management of close contacts in situations of increased epidemiological risk ^4,5.

Bacterial infection is one of the clinical complications of scabies. Scratching repeatedly damages the skin barrier, and it can result in bacterial infection, mostly impetiginsation, which includes both staphylococci and streptococci. As demonstrated by a parasitological study in 2024 on scabies with microscopic confirmation, 35.9% of patients have secondary bacterial infection. It is clinically significant as the infection may progress into deep tissue infection and possibly be a factor in post-streptococcal disease ^6–8.
This report describes an adolescent boarding-school resident with chronic nocturnal pruritus, a close-contact history, and a lower-limb-predominant papulonodular eruption complicated by clinically diagnosed secondary impetiginization. The case highlights the diagnostic challenge of suspected scabies with an atypical active distribution, the importance of recognizing bacterial superinfection in chronically excoriated lesions, and the potential value of concurrent treatment of close contacts and environmental measures in a congregate residential setting.

Case Presentation

An adolescent male student aged 15 years old who lived in an Islamic boarding school was seen on 24 August 2026, with a two-year history of pruritic skin lesions. The adolescent shared a room with three other students. The pruritis initially affected the interdigital area of his hand and the regions below his knees, but later he developed lesions in both lower extremities and dorsum of his feet. He experienced intense pruritis during nighttime, with an NRS score of 7/10. During the last two years, the pruritis and lesions varied and had never healed.

The patient had been consulted before and told that food allergy might be the cause. Afterward, he restricted himself from various foods to no avail. He tried using an unknown lotion that did not show any improvement. He denied having fever or any pain in the lesions. Prior to consultation, some active lesions developed pus and discharged it. As a result of itching and scratching, the lesions had been ruptured or excoriated.

Similar pruritus was noted among two of the patient’s three roommates. There was a past history of close contact with other students who had pruritus as well as sleeping in close proximity to each other. He and other students would often share their sarongs in group activities. Mattresses, pillows, blankets, and clothes were normally personal items and were not usually shared. No one else from the household had similar symptoms.

Physical examination revealed multiple polymorphic lesions with bilateral distribution and relative symmetry over the anterior crura, extending up to the ankles and dorsum pedis. The lesions were comprised of discrete papules and papulonodules that were round to oval and varied in size. Some of the lesions were excoriated and superficially eroded with adherent yellow-brown crust with peripherally located scale. Multiple hyperpigmented macules and papules, which represent post-inflammatory hyperpigmentation, were seen in between. No active interdigital lesions were seen at presentation.

Figure 1. Pretreatment clinical photographs of lower-limb-predominant suspected scabies with secondary  impetiginization.

Multiple discrete papules and papulonodules involving both anterior crura, ankles, and dorsal feet. Several lesions demonstrate excoriation, superficial erosion, adherent yellow-brown crust, and peripheral scale, consistent with clinically suspected secondary impetiginization. Multiple hyperpigmented macules and papules represent post-inflammatory hyperpigmentation. The distribution is bilateral, scattered, and relatively symmetrical.

The clinical diagnosis of probable scabies and superadded impetigo was made. The diagnosis fit the 2020 International Alliance for the Control of Scabies C2 criterion: atypical lesions or atypical distribution along with two history characteristics, which are itch and contact history. Impetigo due to the secondary superficial bacterial infection from preceding pustules/purulent lesions and crusted erosions was clinically diagnosed. Dermoscopy and microscopic skin scraping were not done because the facilities were unavailable.

Other diagnoses to rule out included papular eczema, chronic prurigo, papular urticaria, arthropod bite reaction, and other pruritic papular dermatoses. Scabies was the most probable diagnosis based on nocturnal itching, previous interdigital lesions, contact exposure, and common symptoms of roommates.

Permethrin 5% cream was applied on 24 August 2026 night. The patient was advised to apply the cream to his whole body starting from the neck down, including interdigital spaces, subungual regions, genital area, buttocks, ankles, and feet and leave it for 8-14 hours. The second whole-body treatment with permethrin 5% cream was done on 31 August 2026, 7 days after the first application. Loratadine 10 mg per day orally was prescribed for pruritus.

Localized secondary impetiginization was managed with sterile 0.9% sodium chloride wet compresses applied to crusted and eroded lesions three times daily, followed by topical gentamicin three times daily for seven days. The patient had no fever, lesion-related pain, or clinical features suggestive of cellulitis or systemic bacterial infection. The patient’s three roommates and other close contacts with compatible symptoms received concurrent treatment for suspected scabies. Sarongs, towels, clothing, bedding, and other skin-contact items were cleaned or decontaminated concurrently to reduce the risk of continued transmission and reinfestation. 

During a follow-up on 4 September 2026 conducted 11 days after the initial examination and 4 days following the second permethrin application, there was an alleviation of overall pruritus, both daytime and nighttime, accompanied by improvements in the quality of sleep. There were no new papules, vesicles, nodules, and burrows identified. The examination revealed marked improvement in the crusted and eroded lesions with post-inflammatory hyperpigmentation and little excoriations on the bilateral anterior crura, ankles, and dorsum of feet. There was no notable crusting, no formation of new pustules, and no signs of cellulitis noted. The patient was compliant with the medication and did not experience any adverse effects of the medications including permethrin, loratadine, and topical gentamici.

Figure 2. Post-treatment clinical photographs at follow-up on 4 September 2026

Marked reduction in active inflammatory lesions, erosions, and crusting after topical permethrin 5%, normal saline wet compresses, topical gentamicin, coordinated close-contact treatment, and environmental control measures. Residual multiple hyperpigmented macules and a limited number of excoriated papules are visible on both anterior crura, ankles, and dorsal feet. No obvious new pustules, extensive crusting, or active burrows are seen in the photographed areas

Overall, the clinical course was consistent with resolution of lower-limb-predominant suspected scabies with secondary impetiginization after permethrin 5%, saline compresses, topical gentamicin, simultaneous treatment of close contacts, and environmental decontamination. Parasitological confirmation could not be obtained because dermoscopy and skin-scraping facilities were unavailable.

Table 1 Timeline of events

Discussion

Scabies is caused by the mite Sarcoptes scabiei var. hominis and is transmitted through prolonged skin-to-skin contact or, less commonly, via fomites such as shared bedding and clothing, conditions intrinsic to boarding-school dormitory life⁹. The 2020 IACS Consensus Criteria classify diagnostic certainty into three tiers: Confirmed scabies (A), requiring direct visualization of mites, eggs, or feces via microscopy or dermoscopy; Clinical scabies (B), based on burrows, genital lesions, or typical lesions in a typical distribution with two supportive history features; and Suspected scabies (C), relying on fewer typical findings plus history features such as itch and known contact exposure. In an institutional case report, documenting which IACS level strengthens diagnostic rigor before addressing management ¹⁰.

A key diagnostic pitfall is that secondary bacterial infection presentation, such as impetiginization, crusting, and purulent exudate from excoriated burrows, can obscure the primary scabietic lesions, leading clinicians to misattribute the presentation solely to pyoderma or cellulitis rather than an underlying mite infestation ^11,12, likely seen in this case, where recurrent skin manifestations of itchiness and purulent exudate for 2 years were only treated as skin infections. Without detailed clinical history taking into account, it will still be treated as a skin infection not scabies. With atypical presentation from IACS guidelines, this scabies case is diagnosed as C2 classification. It can be diagnosed with B2 classification with typical distribution on feet and leg, but it has atypical lesion presentation. History taking is noted to have nocturnal itch with positive contact aligned with its environmental demography. Careful analyses of lesion presentation and distribution with history taking is needed to carefully diagnosis a scabies infestation.

First-line pharmacologic therapy as recommended by the 2025 BASHH guideline and many national treatment protocols is dependent upon two drugs: topical permethrin 5% cream or oral ivermectin 200 micrograms/kg with similar effectiveness in clinical trials. In both instances, a second dose 7-14 days after the initial dose must be given in order to eradicate the newly-hatched mites from the eggs missed during the first dosage, as neither of these drugs can destroy all of the eggs. Additionally, adjunct therapies include taking a warm shower using soap before the first application. There is some evidence that hot baths increase systemic absorption without providing any additional treatment benefits, oral antihistamines or calamine lotion for continued pruritus up to 6-12 weeks following treatment even after successful treatment and eradication of the mites, and informing patients that the cessation of itching occurs after the parasitic infection itself has been cured. Failure of the treatment or recurrence after 2 full topical doses, or continued development of new burrows beyond 6-12 weeks should lead to increased therapy with oral ivermectin or combination therapy ^11,12.